Muscle and motor-skill dysfunction in a K+ channel-deficient mouse are notdue to altered muscle excitability or fiber type but depend on the geneticbackground

The voltage-gated K+ channel Kv3.1 is expressed in skeletal muscle and in G ABAergic interneurons in the central nervous system. Hence, the absence of Kv3.1 KC channels may lead to a phenotype of myogenic or neurogenic origin, or both. Kv3.1-deficient (Kv3.1(-/-)) 129/Sv mice display altered contract ile properties of their skeletal muscles and show poor performance on a rot ating rod. In contrast, Kv3.1(-/-) mice on the (129/SvxC57BL/6)F1 backgroun d display normal muscle properties and perform like wild-type mice. The cor relation of poor performance on the rotating rod with altered muscle proper ties supports the notion that the skeletal muscle dysfunction in Kv3.1(-/-) 129/Sv mice may be responsible for the impaired motor skills on the rotati ng rod. Surprisingly, we did not find major differences between wild-type a nd Kv3.1(-/-) 129/Sv skeletal muscles in either the resting or action poten tial, the delayed-rectifier potassium conductance (g(K)) Or the distributio n of fast and slow muscle fibers. These findings suggest that the Kv3.1 Kchannel may not play a major role in the intrinsic excitability of skeletal muscle fibers although its absence leads to slower contraction and relaxat ion and to smaller forces in muscles of 129/Sv Kv3.1(-/-) mice.